Mapping Resistance Genes for Oculimacula Acuformis in Aegilops Longissima
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Theor Appl Genet DOI 10.1007/s00122-014-2361-4 ORIGINAL PAPER Mapping resistance genes for Oculimacula acuformis in Aegilops longissima Hongyan Sheng · Deven R. See · Timothy D. Murray Received: 27 February 2014 / Accepted: 13 July 2014 © Springer-Verlag Berlin Heidelberg 2014 Abstract chromosomal locations as some for resistance to O. yallun- Key message This study identified three QTL confer- dae, except that a QTL for resistance to O. yallundae was ring resistance to Oculimacula acuformis in Aegilops found in chromosome 7Sl but not for O. acuformis. Thus, longissima and their associated markers, which can be it appears that some genes at the same locus in Ae. long- useful in marker-assisted selection breeding for eyespot issima may control resistance to both eyespot pathogens. resistance. QTL effective against both pathogens will be most useful Abstract Oculimacula acuformis is one of two species for breeding programs and have potential to improve the of soilborne fungi that cause eyespot of wheat, the other effectiveness and genetic diversity of eyespot resistance. being Oculimacula yallundae. Both pathogens can coex- ist in the same field and produce elliptical lesions on stem bases of wheat that are indistinguishable. Pch1 and Pch2 Introduction are the only two eyespot resistance genes readily avail- able to wheat breeders, but neither provides complete Eyespot, a stem base disease of wheat, is caused by Ocu- control. A new source of eyespot resistance was identified limacula acuformis Crous & W. Gams (syn: Tapesia acu- from Aegilops longissima (2n 14, SlSl), a wild relative formis, Wallwork & Spooner) and O. yallundae Crous & = of wheat. Three QTL for resistance to O. acuformis were W. Gams (syn: T. yallundae) (Crous et al. 2003). These mapped in chromosomes 1Sl, 3Sl, and 5Sl using a recom- fungi often coexist in the same field and cause eye-shaped binant inbred line population developed from the cross Ae. elliptical lesions at the stem bases that are indistinguish- longissima accessions PI 542196 (R) PI 330486 (S). able. Eyespot occurs in many cool and wet wheat growing × The three QTL explained 66 % of phenotypic variation areas in the world. In the USA, eyespot is a chronic and by β-glucuronidase score (GUS) and 84 % by visual rat- economically important disease of winter wheat in the ing. These QTL had LOD values of 10.6, 8.8, and 6.0 for Pacific Northwest (PNW) region including Idaho, Oregon GUS score, and 16.0, 10.0, and 13.0 for visual rating. QTL and Washington. Severe eyespot results in stem breakage associated with resistance to O. acuformis have similar and multi-directional lodging in the field (Maloy and Inglis 1993). Up to 50 % yield reduction has been documented in severely affected fields (Murray 2010). Communicated by Frank Ordon. Although eyespot was controlled with fungicides for many years, limiting input costs, environmental concerns, * H. Sheng · D. R. See · T. D. Murray ( ) and fungicide resistance resulted in the need for planting Department of Plant Pathology, Washington State University, Pullman, WA 99164-6430, USA resistant cultivars. Resistance to eyespot has been investi- e-mail: [email protected] gated since the pathogen was first described (Sprague and Fellowes 1934). Discovery of the wheat relative Aegilops D. R. See ventricosa. Tausch (2n 28, DDMvMv) (syn. Triticum US Department of Agriculture, Agricultural Research Service = (USDA-ARS), Wheat Genetics, Quality Physiology and Disease ventricosum (Tausch) Ces.) by Sprague (1936) led to the Research Unit, Pullman, WA 99164-6430, USA introgression of eyespot resistance gene Pch1 into common 1 3 Theor Appl Genet wheat (Kimber 1967; Doussinault et al. 1983). Pch1 is the Aegilops longissima Schweinf. & Muschl. (2n 2x 14, = = most effective resistance gene to eyespot to date. It is a sin- SlSl), a diploid species in the section Sitopsis of Aegilops L. gle dominant gene mapped to the distal end of the long arm (Van Slageren 1994), is a distant relative of wheat and poten- of chromosome 7D (Worland et al. 1988). Through breed- tial donor of genes for wheat cultivar improvement, including ing line VPM-1 (Ventricosa Persicum Marne), Pch1 disease resistance (Friebe et al. 1993). In previous studies, × × has been incorporated into several commercial wheat cul- Ae. longissima was identified as containing a new source of tivars for use in the US PNW. Madsen, the first eyespot eyespot resistance (Sheng and Murray 2013). Multiple genes resistant line in the US PNW, was released in 1988 by the in the Sl genome were found to be responsible for genetic USDA-ARS and Washington State University winter wheat control of eyespot resistance and some of them reacted dif- breeding program at Pullman, WA (Allan et al. 1989). It has ferently from O. yallundae and O. acuformis (Sheng and been widely grown in the PNW for more than two decades Murray 2013). A genetic linkage map composed of 169 (Murray 2010). Lind (1999) found that Pch1 resistance was wheat microsatellite markers (SSR markers) was constructed more effective in early plant growth stages than at the adult with the Sl genome with a recombinant inbred line popula- stage. Burt et al. (2010) found that Pch1 conferred resist- tion of Ae. longissima (Sheng et al. 2012). Furthermore, four ance to both O. acuformis and O. yallundae at the seedling QTL conferring resistance to O. yallundae were mapped in stage. chromosome 1Sl, 3Sl, 5Sl, and 7Sl (Sheng et al. 2012). The French variety Cappelle Desprez containing Pch2 is objective of this study was to determine the genetic control the only known source of eyespot resistance from hexa- of resistance to O. acuformis in the Sl genome of Ae. longis- ploid wheat (Hollins et al. 1988). Law et al. (1976) found sima by QTL mapping using wheat SSR markers. This work evidence that eyespot resistance in Cappelle Desprez is will contribute to the long-term goal of transferring new eye- located on chromosomes 1A, 2B, 5D, and 7A, with a major spot resistance genes to wheat. component on 7A. Pch2 was later mapped to the distal por- tion of 7AL with RFLP markers (de la Peña et al. 1997). Recently, a major QTL associated with eyespot resistance Materials and methods was mapped on chromosome 5AL of Cappelle Desprez (Burt et al. 2011). Although Pch2 is less effective than Mapping population Pch1 (Johnson 1992), Cappelle Desprez has been grown extensively and its resistance has been transferred to many Aegilops longissima accessions PI 542196 and PI 330486 other wheat varieties in Europe since the 1950s (Hollins provided by the USDA National Small Grains Collection et al. 1988). Burt et al. (2010) found that Pch2 was signifi- (NSGC) were identified as resistant and susceptible to cantly more effective against O. acuformis than O. yallun- both O. yallundae and O. acuformis, respectively (Sheng dae at the seedling stage and that the QTL on chromosome and Murray 2013), and were selected as the resistant 5A conferred resistance to both pathogens at the seedling and susceptible parents for development of a recombi- and adult stages (Burt et al. 2011). nant inbred line (RIL) population (Sheng et al. 2012). Although Pch1 and Pch2, along with the QTL on 5AL The population was developed to F8 through single-seed of Cappelle Desprez, have been used to effectively pro- descent. tect wheat from eyespot disease, none of them provides complete resistance to eyespot when used alone. Addi- Phenotypic evaluation tional resistance genes are desired for incorporation into adapted wheat cultivars to improve the effectiveness and One-hundred and seventy-eight F RIL of PI 542196 (R) 8 × diversity of resistance genes. Wild species of wheat have PI 330486 (S) were tested for resistance to O. acuformis received considerable attention as sources of eyespot resist- in two growth chamber (Controlled Environments Lim- ance (Jones et al. 1995). A single dominant gene, Pch3 or ited, Winnipeg, Manitoba, Canada) experiments. The PchDv, was mapped to chromosome 4VL of Dasypyrum parent lines and the winter wheat cultivar Madsen were villosum because of its eyespot resistance (Yildirim et al. included in the experiments as controls. Each experiment 1998), but the gene has not been used commercially. Uslu was a randomized complete block (RCB) design with two et al. (1998) found multiple resistance genes in D. villo- subsamples and three blocks. Thus, a total of 12 plants per sum chromosomes 4V and 5V to O. yallundae and O. acu- line were evaluated for phenotypic variation. The planting formis, respectively; the first report showing differential method and growth chamber conditions were the same as resistance to these two pathogens. Burt et al. (2010) also for the phenotypic evaluation of F5 RIL to O. yallundae demonstrated that Triticum monococcum accessions had (Sheng et al. 2012). significantly different resistance reactions to O. yallundae Disease evaluation was conducted after inoculating and O. acuformis. seedlings with β-glucuronidase (GUS) transformed O. 1 3 Theor Appl Genet acuformis isolates tph98-2-34A, tph98-2-34D, tph98-2- WinQTLCart V2.5 (Wang et al. 2010). Composite Interval 34E, and tph98-1-54aa (de la Peña and Murray 1994). Mapping was conducted to identify the chromosome loca- Each two-leaf stage seedling was inoculated twice with tions of major QTL associated with resistance to O. acu- 250 µl slurry of conidia containing 1.2 105 conidia per formis (Sheng et al. 2012). × ml (Sheng et al. 2012). Visual disease ratings were performed at growth stage 23–25 (Zadoks et al. 1974), about 8 weeks after inocula- Results tion. All tillers (2–4) of each plant were cut into a 3 cm- long section above the soil line. After washing in water Phenotypic evaluation to remove soil, stems were evaluated visually for disease severity on a 0–4 scale, where 0 healthy to 4 nearly Based on the F ratio test, the error variances of GUS scores = = dead (Sheng et al.